Cancer causes and Prevention

How bacteria could cause cancer:
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(Source:- https://www.sciencedirect.com
Titled:- How bacteria could cause cancer one step at a time-ScienceDirect)

Abstract:-

Helicobacter pylori highlighted the potential for bacteria to cause cancer. It is becoming clear that chronic infection with other bacteria, notably Salmonella typhi, can also facilitate tumour development. Infections caused by several bacteria (e.g. Bartonella spp., Lawsonia intracellularis and Citrobacter rodentium) can induce cellular proliferation that can be reversed by antibiotic treatment. Other chronic bacterial infections have the effect of blocking apoptosis. However, the underlying cellular mechanisms are far from clear. Conversely, several bacterial toxins interfere with cellular signalling mechanisms in a way that is characteristic of tumour promoters. These include Pasteurella multocida toxin, which uniquely acts as a mitogen, and Escherichia coli cytotoxic necrotizing factor, which activates Rho family signalling. This leads to activation of COX2, which is involved in several stages of tumour development, including inhibition of apoptosis. Such toxins could provide valuable models for bacterial involvement in cancer, but more significantly they could play a direct role in cancer causation and progression.

Section snippets:
Epidemiology of bacterial infection and carcinogenesis
The relationship between H. pylori and carcinogenesis is not straightforward 4., 5.. Much of the evidence to link H. pylori with carcinogenesis is epidemiological and thus open to different interpretations. This is further complicated by the diversity of H. pylori isolates, which mutate and evolve within an individual such that any one person is infected with several H. pylori quasispecies, each having a different virulence potential. Consequently, it is difficult to determine which virulence

Immunological mechanisms involved in the induction of carcinogenesis:-

Although the linkage between H. pylori infection and gastric cancer is convincing, the molecular mechanism or mechanisms responsible are unclear, and both bacterial and host factors are implicated. One view is that increased inflammation generates reactive oxygen and nitrogen intermediates that might lead directly to DNA damage 23., 24.. The role of the immune response, in particular a CD4+ T cell response, is supported by work using H. felis infection in mice, although it is noteworthy that

Proliferative infections:-

It is known that protracted growth stimulation can promote tumour formation by facilitating the acquisition of mutations in genes encoding the signalling and cell cycle proteins that control proliferation. Several bacterial infections promote cell proliferation and so could increase the rate of cell transformation. H. pylori activates several genes known to be associated with carcinogenesis, such as cyclooxygenase 2 (COX2) [31], c-Jun amino-terminal kinase (JNK) [27] and phospholipase A2 [32].

The suppression of apoptosis
An important mechanism by which transformed cells can normally be prevented from proliferating and developing into tumours is through the induction of pre-programmed cell death or apoptosis (Fig. 1). Apoptosis results from several different extracellular stimuli but, in the case of potential cancer cells, the release of the serine protease granzyme B and tumour necrosis factor α (TNF-α) from activated CD8+ T cells are important mechanisms. Tumour cells can have abnormal expression levels of Bacterial toxins and Rho protein activation:-

The Rho family of small GTPases act as key molecular switches that integrate signals from several different signal transduction pathways. These also control and regulate movement and other aspects of cytoskeletal changes. It is becoming clear that these proteins can play a key role in carcinogenesis [57], either through their aberrant activation, which can result in uncontrolled proliferation and growth transformation, or by regulating processes downstream of other oncogenes such as Ras.

Conclusion:-

The number of examples where epidemiological evidence has linked prior and chronic bacterial infection to tumour formation is growing, but the molecular mechanisms involved remain far from clear. For example, despite much research, it remains uncertain which of the many virulence factors produced by H. pylori have most significance for cancer development. Conversely, several bacteria and their products have properties that could advance carcinogenesis although there is currently no known link

(Author links open overlay panelAlistair J.LaxWarrenThomas
https://doi.org/10.1016/S0966-842X(02)02360-0)

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cancer-causing bacteria and viruses:-
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(Source:- https://feedhutch.org
Titled:- What we’re learning about cancer-causing bacteria and viruses)

Unusual links between our microbiome and cancer highlighted at 2017 American Society of Preventive Oncology
MARCH 15, 2017 • BY RACHEL TOMPA / FRED HUTCH NEWS SERVICE
Dr. Meredith Hullar
"Gone are the days of one organism, one disease. We’re really looking at how a whole community of microbes influences disease risk,” said Fred Hutch's Dr. Meredith Hullar, who attended this week's ASPO conference in Seattle.
Photo by Robert Hood / Fred Hutch News Service
For as long as humans have walked the earth, we’ve been accompanied by microscopic beings that are part of our bodies but not ourselves. The viruses and bacteria that coexist with humans have shaped who we are, but that doesn’t mean they are all benevolent.

As research presented at this week’s 2017 American Society of Preventive Oncology meeting in Seattle showed, viewing our microbes as wholly good or bad might be an oversimplification.

Dr. Meredith Hullar is a researcher at Fred Hutchinson Cancer Research Center who studies the gut microbiome — the collection of trillions of bacteria that inhibit our digestive tract — and its complex interplay with diet and cancer risk. She spoke at the meeting Monday about her research and that of others who are looking at how gut bacteria can increase or decrease colorectal cancer risk.

Gut bacteria can alter cancer risk up or down
“Gone are the days of one organism, one disease. We’re really looking at how a whole community of microbes influences disease risk,” Hullar said. “For example, scientists are looking at how the metabolism of the microbiome — all of the members of the microbial community — influences its host,” she said. Researchers are exploring questions such as whether the microbiome produces metabolites that promote tumor growth or may prevent cancer.

There are several different types of human bacteria that can directly fuel colorectal cancer risk, Hullar said. Those include the bacterial species Streptococcus gallolyticus and Fusobacterium nucleatum, as well as certain types of E. coli and conglomerate communities of bacteria that form layers in the gut that are called biofilms. All of these microbes act in different ways on the cells that line our gut to increase risk of tumor formation, she said.

But interestingly, many other types of gut bacteria can alter cancer risk — either up or down — through indirect routes that involve what we eat.

Because these bacteria help digest our food, what we eat influences what they excrete in our gut. Some microbial byproducts — such as those produced when processed meat or high-protein foods are digested — increase cancer risk. Compounds formed in the gut by bacteria during the digestion of a high-fiber food — for example, cruciferous vegetables such as broccoli — seem to be linked to a lower risk of colorectal cancer, Hullar said. She and her colleagues are studying the different microbial communities in people with high or low levels of one of those compounds linked to a lower risk of cancer, known as enterolignans. They are now researching whether changing people’s diets changes the amount of enterolignans they produce and how the human cells that line the gut may respond to those compounds in cancer prevention.

Two deadly pathogens:-

Although these complex bacterial communities seem to have equally complex relationships with cancer risk, there’s at least one bacterium whose link to cancer is somewhat more straightforward. The bacterium Helicobacter pylori — which colonizes in the stomachs of about two thirds of people worldwide — is directly linked to stomach cancer, the fifth most common cancer in the world and the third most common cause of cancer-related death, said microbiologist Dr. Meira Epplein of Vanderbilt University at Monday’s session.

Although eradicating the bacterium may stem stomach cancer, it’s not yet clear who should be targeted, Epplein said. Her team is studying communities in the Southeastern U.S. who have higher than average levels of H. pylori infection.

But even here, the picture is nuanced. Most people infected with the bacterium don’t develop stomach cancer, and H. pylori infection also seems to reduce the risk of a type of esophageal cancer, Epplein said, so more research is needed.

Stopping hepatitis C from turning deadly:-

Dr. Lesley Miller of Emory University dropped a statistic that she felt hasn’t reached enough of the public — that hepatitis C virus kills more people in the U.S. than any other infectious disease, including HIV. Up to 4 million people in the U.S. are infected with the virus, Miller said, and it’s incredibly deadly. If unchecked, it can lead to cirrhosis and liver cancer, which is very difficult to treat.

But the infection is very treatable if diagnosed early enough, she said. And in 2012, the Centers for Disease Control and Prevention recommended that all baby boomers, the segment of the population that has the most hepatitis-C infections, be screened for the virus. The infection can be cleared with a simple (if expensive) course of oral antivirals before it progresses to cancer.

“It’s really frustrating to see a case of cancer that’s completely preventable, if we could have caught the infection and treated it earlier,” Miller said.

HPV vaccine: some good news, some bad news:-

Public health researchers from around the country convened at Monday’s meeting to present their latest findings on the HPV vaccine — who’s getting it, who’s not, do parents who decline the vaccine for their children ever change their minds, and is the vaccine doing any good?

The HPV vaccine may be one of the best cancer prevention methods to come onto the market in the past few decades. It’s highly effective at preventing the strains of HPV that cause nearly all cases of cervical cancer and many other anoge***al cancers — plus head and neck cancers. The vaccine, which was approved for girls in 2006 and for boys in 2009, works best if people are vaccinated before they’re exposed to the virus. Since HPV is s*xually transmitted, that means the vaccine is recommended for pre-adolescent children aged 11-12 — before they’re s*xually active. The vaccine is also approved for teenagers and young adults in the U.S. up to age 26. (Children under 14 need just two doses of the vaccine; those 15 and older still need three doses.)

And in countries where most kids get the vaccine, it’s working. In Australia, which has a nationwide vaccination program, cases of ge***al warts, an earlier sign of HPV infection than the virus-linked cancers, dropped more than 90 percent in young women after the vaccine was implemented. But clinicians and researchers alike have been dismayed by the vaccine’s low uptake rate in the U.S. In 2015, only 42 percent of girls and 28 percent of boys had received the full vaccine series.

Many researchers are trying to boost that number, including some who presented Monday at ASPO.

But the results of their efforts have not always been so easy to understand, they said. Dr. Nora Henrikson of Kaiser Permanente Washington Health Research Institute (formerly the Group Health Research Institute) in Seattle presented results from a study in which parents of unvaccinated children aged 10 and older received a letter with information about the vaccine written by a pediatrician and nurse. Starting when the children turned 11 and were eligible for the vaccine, they also got automated phone call reminders and the option to opt in to a text-reminder system.

Overall, the Kaiser study found a slight boost to vaccine rates, Henrikson said. In surveys, the parents said they liked the mailed information, and 23 percent of those who received a letter and phone-call reminder brought their child in for the first vaccine dose within three months of the reminder, as compared to 18 percent of parents who didn’t get a phone or mail prompt.

Parents with young adolescents who haven’t yet gotten their kids vaccinated aren’t necessarily going to be lifelong vaccine refusers, as Henrikson’s study found. That squares with a study led by Dr. Melanie Kornides from Harvard Medical School, who asked: Do parents who actively refuse the HPV vaccine for their children ever change their minds? Using an online survey, she and her colleagues looked at close to 500 parents of adolescents who were eligible and had access to the HPV vaccine and had refused the vaccine at a well-child checkup. Surprisingly, 45 percent of those parents later changed their mind and said yes to the vaccine. Another 24 percent said they were planning to get their child vaccinated in the coming year.

This is an important message to send to health care providers, Kornides said, many of whom have reported frustrating encounters with parents who refuse vaccination. Previous studies have found that providers spend extra time and resources on these families and the providers report that they feel the time is wasted because they don’t think the parents will change their minds.

But the Harvard study showed not only that close to half of these parents will reverse course, but that they’re influenced by the information they get from their providers. Parents who reported high satisfaction with the provider communication were more than three times as likely to agree to the vaccine later than parents who weren’t satisfied. And providers who brought up the HPV vaccine again in a later visit, even after the parents had already refused, were more than twice as likely to change the parents’ minds.

“Providers really should be bringing the vaccine up again, because many of these people will go on to get it,” Kornides said.

Even though vaccine refusal and the low uptake may be a hard nut to crack, the reasons parents gave for changing their mind were not complex, the researchers found. Close to half of those who changed their mind said it was simply because their child got older. And approximately a third also said learning more about the vaccine and getting good information from their providers influenced their decision to accept vaccination.

Other highlights from the HPV-associated cancers talks included:

Research from the University of Texas Medical Branch that found cervical-cancer incidence rates have decreased in young women since the vaccine has been implemented in the U.S. Even though this study doesn’t definitively prove that the vaccine is linked to the decrease since the population-wide cancer registry doesn’t track HPV vaccination, it’s an encouraging result that even at low levels of uptake, the vaccine is working as intended, said Dr. Fangjian Guo, who led the study.
Dr. Joel Palefsky of the University of California, San Francisco described research showing that HPV-associated a**l cancers and precancers are prevalent and on the rise in HIV-infected men who have s*x with men and women. Although a**l-cancer screening guidelines are not as definitive as those for cervical cancer, the disease seems to follow the same course, Palefsky said. His team is conducting a study to see if removing precancerous lesions prevents a**l cancer in the same way it does for cervical cancer.
Dr. Roshan Bastani of the University of California, Los Angeles led a phone-based intervention study to increase HPV vaccination. Bastani’s study was aimed at low-income, ethnic minority families in Los Angeles who had called a health hotline. Interestingly, her study found that both the control group who didn’t receive information about the vaccine and the group who did increased their child-vaccination rates. Bastani thinks that’s because the survey her team conducted to enroll people in the study was enough to give them the extra information they needed to get their children vaccinated. For her, this was good news: “In some populations where the [vaccination] rate is very low, you can get the low-hanging fruit with something that is very minimal,” she said. “So we need to all do that.”

(Rachel Tompa is a former staff writer at Fred Hutchinson Cancer Center. She has a Ph.D. in molecular biology from the University of California, San Francisco and a certificate in science writing from the University of California, Santa Cruz. Follow her on Twitter .)



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How cancer starts, grows and spreads:-
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(Source:- https://cancer.ca

Titled:- How cancer starts, grows and spreads)

Our bodies are made up of trillions of cells grouped to form tissues and organs. Genes
inside the nucleus of each cell tell it when to grow, work, divide and die. Normally, our cells follow these instructions and we stay healthy.

But when there is a change in our DNA or damage to it, a gene can mutate. Mutated genes don’t work properly because the instructions in their DNA get mixed up. This can cause cells that should be resting to divide and grow out of control, which can lead to cancer.

How cancer starts:-

When genes work properly, they tell cells when it is the right time to grow and divide. When cells divide, they make exact copies of themselves. One cell divides into 2 identical cells, then 2 cells divide into 4, and so on. In adults, cells normally grow and divide to make more cells only when the body needs them, such as to replace aging or damaged cells.

But cancer cells are different. Cancer cells have gene mutations that turn the cell from a normal cell into a cancer cell. These gene mutations may be inherited, develop over time as we get older and genes wear out, or develop if we are around something that damages our genes, like cigarette smoke, alcohol or ultraviolet (UV) radiation from the sun.

A cancer cell doesn’t act like a normal cell. It starts to grow and divide out of control instead of dying when it should. They also don’t mature as much as normal cells so they stay immature. Although there are many different types of cancer, they all start because of cells that are growing abnormally and out of control. Cancer can start in any cell in the body.

How cancer grows;-

Gene mutations in cancer cells interfere with the normal instructions in a cell and can cause it to grow out of control or not die when it should. A cancer can continue to grow because cancer cells act differently than normal cells. Cancer cells are different from normal cells because they:divide out of control
are immature and don’t develop into mature cells with specific jobs avoid the immune system
ignore signals that tell them to stop dividing or to die when they should don’t stick together very well and can spread to other parts of the body through the blood or lymphatic system
grow into and damage tissues and organs
As cancer cells divide, a tumour will develop and grow. Cancer cells have the same needs as normal cells. They need a blood supply to bring oxygen and nutrients to grow and survive. When a tumour is very small, it can easily grow, and it gets oxygen and nutrients from nearby blood vessels.

But as a tumour grows, it needs more blood to bring oxygen and other nutrients to the cancer cells. So cancer cells send signals for a tumour to make new blood vessels. This is called angiogenesis and it is one of the reasons that tumours grow and get bigger. It also allows cancer cells to get into the blood and spread more easily to other parts of the body. There is a lot of research that is looking at using drugs that stop blood vessel growth (called angiogenesis inhibitors), causing a tumour to stop growing and even shrink.

How cancer spreads:-

As a tumour gets bigger, cancer cells can spread to surrounding tissues and structures by pushing on normal tissue beside the tumour. Cancer cells also make enzymes that break down normal cells and tissues as they grow. Cancer that grows into nearby tissue is called local invasion or invasive cancer.

Diagram of how cancer spreads
Diagram of how cancer spreads
Cancer can also spread from where it first started to other parts of the body. This process is called metastasis. Cancer cells can metastasize when they break away from the tumour and travel to a new location in the body through the blood or lymphatic system.

Where cancer can spread and staging:-

Most cancers have a tendency to spread to certain areas of the body. This has helped doctors develop staging systems that are used to classify cancers based on information about where the cancer is in the body and if it has spread from where it started. Many cancers follow a staging system from 1 to 4 that is usually given in Roman numerals I, II, III or IV. Knowing how a cancer spreads and where a cancer may spread helps doctors predict how the cancer will grow. This also helps them plan treatment and give appropriate supportive care.

Cancer can spread anywhere in the body, but it’s most likely to spread to lymph nodes, bones, the brain, the liver or the lungs.

Why does cancer sometimes come back?:-

Cancer sometimes comes back after treatment. This is called a recurrence. Even if one cancer cell is left behind, it can grow and divide to become a new tumour. A new tumour can start to grow in the same area of the body where the cancer first started, or the cancer may have spread through the blood or lymphatic system to another part of the body, where it grows into a new tumour. This is why doctors sometimes use another treatment right after the first treatment, such as giving chemotherapy after surgery. This is called adjuvant therapy. The goal of adjuvant therapy is to help prevent the cancer from coming back in case some cancer cells are left behind in the body.

In some cases, treatment may stop working (become resistant) so cancer cells are no longer being destroyed. So cancer that was shrinking or had disappeared may start to grow again and get bigger. This can happen when the genes inside cancer cells mutate. Some gene mutations make cancer cells resistant to chemotherapy and other drug treatments. If you become resistant to a treatment, your doctor may suggest that you try another one.

Cure or remission:-

Many cancers can be cured with treatment. But cancer that is thought to be cured can still come back even years later. This is why some doctors prefer to say that the cancer is in remission. Remission means there are fewer signs and symptoms of a disease (such as cancer) or that they have completely gone away.

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